Tweety-Homolog 1 Facilitates Pain via Enhancement of Nociceptor Excitability and Spinal Synaptic Transmission
| Autor: | Hua Han, Sui-Bin Ma, Wen-Juan Han, Fei Wang, Min-Hua Zheng, Ceng Luo, Dong-Hao Wang, Hai-Ning Wu, Wang Fudong, Shengxi Wu, Zhen-Zhen Li, Rou-Gang Xie, Xiu-Li Cao, Wu Wenbin |
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| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Physiology Postsynaptic Current Pain Biology Neurotransmission Synaptic Transmission 03 medical and health sciences chemistry.chemical_compound Mice 0302 clinical medicine medicine Animals Periaqueductal Gray Neurotransmitter Sensitization Neurons General Neuroscience Membrane Proteins Nociceptors Long-term potentiation General Medicine 030104 developmental biology medicine.anatomical_structure Nociception chemistry nervous system Nociceptor Excitatory postsynaptic potential Original Article Neuroscience 030217 neurology & neurosurgery |
| Zdroj: | Neurosci Bull |
| Popis: | Tweety-homolog 1 (Ttyh1) is expressed in neural tissue and has been implicated in the generation of several brain diseases. However, its functional significance in pain processing is not understood. By disrupting the gene encoding Ttyh1, we found a loss of Ttyh1 in nociceptors and their central terminals in Ttyh1-deficient mice, along with a reduction in nociceptor excitability and synaptic transmission at identified synapses between nociceptors and spinal neurons projecting to the periaqueductal grey (PAG) in the basal state. More importantly, the peripheral inflammation-evoked nociceptor hyperexcitability and spinal synaptic potentiation recorded in spinal-PAG projection neurons were compromised in Ttyh1-deficient mice. Analysis of the paired-pulse ratio and miniature excitatory postsynaptic currents indicated a role of presynaptic Ttyh1 from spinal nociceptor terminals in the regulation of neurotransmitter release. Interfering with Ttyh1 specifically in nociceptors produces a comparable pain relief. Thus, in this study we demonstrated that Ttyh1 is a critical determinant of acute nociception and pain sensitization caused by peripheral inflammation. |
| Databáze: | OpenAIRE |
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